Cell membranes contain numerous nanoscale conductors in the form of ion channels and ion pumps [1][2][3][4] that work together to form ion concentration gradients across the membrane, which can be triggered to release an action potential (AP) 1,5 . We ask if artificial cells can be built to utilize ion transport as effectively as natural cells. Here we used the electrogenic cell (electrocyte) of an electric eel to model the formation of AP by tracking the conversion of ion concentration gradients into APs across the different nanoscale conductors. Using the parameters extracted from the model, we designed an artificial cell based on an optimized selection of conductors. The resulting cell is similar to the electrocyte but has higher power output density and greater energy conversion efficiency. We suggest methods for producing these artificial cells that have applications in powering medical implants and other tiny devices.The electrocyte in an electric eel (Electrophorus electricus) can generate potentials of about 600V 2,3,6 to stun prey and ward off predators (Fig. 1a). The transmembrane proteins in the electrocytes are asymmetrically distributed across two primary membranes, one innervated and the other non-innervated (Fig. 1b), and are separated by an insulating septa (wall). The non-innervated membrane has numerous sodium potassium ATPase pumps (Na + /K + ) and both K + and chloride (Cl − ) channels. The innervated membrane contains high densities of acetylcholine receptors (AChRs), voltage-gated Na+ channels (which are responsible for activating APs), voltage-gated K + channels (Kvs) 7 , inward rectifier K + channels (Kirs, which are ion channels that stop ion flow when the membrane is depolarized) 6 and leak channels.When the chemical agonist, acetylcholine (ACh), is released into the junction between the AChR and another nearby excitable cell (synapse), AChRs bind with ACh and become permeable to the cations, Na + and K + . This opens the AChRs and depolarizes the innervated membrane, raising the probability that voltage-gated Na + channels will open (Fig. 1c) 3,6,8 . Depolarization causes the normally negative innervated cell membrane potential to become positive with respect to the potential on the non-innervated membrane. With Na + flowing into the cell, the innervated membrane potential further increases, causing the opening of additional voltage-gated Na + channels. This cascade of AChRs opening large number of Na + channels results in AP formation on the innervated membrane. The Kir channels are closed during this stage, which speeds the increase of the membrane potential. The maximum innervated 5,6 . The non-innervated membrane potential remains at approximately −85mV due to ATPase, K + channel and Cl − activity 2,5,6 . After the peak of the AP, the innervated membrane is repolarized with the inactivation of Na + channels 8 and the opening of Kir and Kvs channels. Ion flux through leak channels further expedites the restoration of membrane potential to the resting state (−85mV). The ion ...